Evidence map›Paper›PMID 29282359›Full record

ReviewProstate cancer and prostatic diseases2018

The molecular biology of prostate cancer: current understanding and clinical implications.

Jason Gandhi, Adil Afridi, Sohrab Vatsia, Gargi Joshi, Gunjan Joshi, Steven A Kaplan, Noel L Smith, Sardar Ali Khan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Prostate cancer and prostatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 3 pooled it
6.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 3 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  4. RAB40C regulates SNX9 stabilityCentral-European journal of immunology · 2026
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  13. PROTACs in the Management of Prostate Cancer.Molecules (Basel, Switzerland) · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 6 institutions in 2 countries.

Jason GandhiDepartment of Physiology and Biophysics, Stony Brook University School of Medicine, Stony Brook, NY, USA.
Adil AfridiDepartment of Physiology and Biophysics, Stony Brook University School of Medicine, Stony Brook, NY, USA.
Sohrab VatsiaDepartment of Cardiothoracic Surgery, Lenox Hill Hospital, New York, NY, USA.
Gargi JoshiDepartment of Physiology and Biophysics, Stony Brook University School of Medicine, Stony Brook, NY, USA.
Gunjan JoshiDepartment of Internal Medicine, Stony Brook Medicine at Southampton Hospital, Southampton, NY, USA.
Steven A KaplanDepartment of Urology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Noel L SmithFoley Plaza Medical, New York, NY, USA.
Sardar Ali KhanDepartment of Physiology and Biophysics, Stony Brook University School of Medicine, Stony Brook, NY, USA. skysalik@gmail.com.
Stony Brook Medicine · USStony Brook University · USFoley Hoag (United States) · USIcahn School of Medicine at Mount Sinai · USLenox Hill Hospital · USSt. George's University · GD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWith continuous progress over the past few decades in understanding diagnosis, treatment, and genetics, much has been learned about the prostate cancer-diagnosed genome.

methodsA comprehensive MEDLINE® and Google scholar literature search was conducted using keyword variations relating to the genetics of prostate cancer such as chromosomal alterations, androgen receptor, castration-resistant, inheritance, polymorphisms, oncogenes, metastasis, biomarkers, and immunotherapy.

resultsTraditionally, androgen receptors (AR) have been the focus of research. Recently, identification of recurrent chromosomal alterations that lead to either multiplication of regions (gain-of-function) or deletion of regions (loss-of-function) has opened the door to greater genetic accessibility. These chromosomal aberrations lead to variation in copy number and gene expression. Some of these chromosomal alterations are inherited, while others undergo somatic mutations during disease progression. Inherited gene mutations that make one susceptible to prostate cancer have been identified with familial-linked studies. Somatic genes that progress tumorigenesis have also been identified. Research on the molecular biology of prostate cancer has characterized these genes into tumor suppressor genes or oncogenes. Additionally, genome-wide assay studies have identified many high-risk single-nucleotide polymorphisms recurrent throughout the prostate cancer-diagnosed genome. Castration-resistant prostate cancer is the most aggressive form of prostate cancer, and its research has elucidated many types of mutations associated with AR itself, including enhanced expression and amplification, point mutations, and alternative splicing. Understanding the molecular biology of prostate cancer has permitted more accurate identification using advanced biomarkers and therapy for aggressive forms using immunotherapy.

conclusionsAn age-related disease, prostate cancer commands profound attention. With increasing life expectancy and the continuous pursuit of it, prostate cancer is a powerful obstacle best defeated using targeted therapies specifically designed for the unique molecular profile of the malignancy.

Indexed as

Drug Resistance, NeoplasmGenetic Predisposition to DiseaseGenome, HumanHumansMaleMutationOrchiectomyPolymorphism, Single NucleotideProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAR protein, humanReceptors, Androgen

Identifiers

PMID29282359
OpenAlexW2777231946

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.